The aim of this research is to obtain basic information concerning how the bioenergetic apparatus and reactions in mammalian mitochondria change with the age of Syrian golden hamsters on a "common" diet compared to animals rationed with a high-fat and high-cholesterol diet. The survival curves or mortality rates for these two groups of hamsters will be recorded with major classification of the causes of the deaths. At 1.5 to 4 week intervals from new born to the death of all animals, we will study all bioenergetic components, the partial and complete electron transport and energy-linked reactions, such as States 3 and 4 oxidation, respiratory control, ADP/O ratio, ATPase, the activities of cytochrome oxidase, and NADH- and succinate-cytochrome c reductases, etc. The mitochonria of brain, heart, and liver will be used. The effect of aging on the number or size of mitochondria, if any will be studied by the determination of the percent of mitochondrial protein per total tissue protein. When the focal points due to aging and/or diet are narrowed down or located, we will endeavor an in-depth study to find out "why". Attempts will be made to construct mathematical models to simulate the aging of hamsters. If successful, predication may thus be made. Our premise is that aging can be affected by dietary intake and old age or senescence may be considered a metabolic disease. Rejuvenation may be accomplished clinically and prevented effectively. Our rationale is that in order to achieve this goal to meet increasing demand for older people in the next century because of the changing trends of population growth and socio-economic systems, the cause of so-called senescence must be first uncovered and then remedied.